Search

Lung cancer is a serious health problem, since it is one of the leading causes for death worldwide. Molecular-cytogenetic studies could provide reliable data about genetic alterations which could be related to disease pathogenesis and be used for better prognosis and treatment strategies. We performed whole genome oligonucleotide microarray-based comparative genomic hybridization in 10 samples of non-small cell lung cancer. Trisomies were discovered for chromosomes 1, 13, 18 and 20. Chromosome arms 5p, 7p, 11q, 20q and Хq were affected by genetic gains, and 1p, 5q, 10q and 15q, by genetic losses. Microstructural (<5 Mbp) genomic aberrations were revealed: gains in regions 7p (containing the epidermal growth factor receptor gene) and 12p (containing KRAS ) and losses in 3p26 and 4q34. Based on high amplitude of alterations and small overlapping regions, new potential oncogenes may be suggested: NBPF4 (1p13.3); ETV1 , AGR3 and TSPAN13 (7p21.3-7p21.1); SOX5 and FGFR1OP2 (12p12.1-12p11.22); GPC6 (13q32.1). Significant genetic losses were assumed to contain potential tumour-suppressor genes: DPYD (1p21.3); CLDN22 , CLDN24 , ING2 , CASP3 , SORBS2 (4q34.2-q35.1); DEFB (8p23.1). Our results complement the picture of genomic characterization of non-small cell lung cancer.

The aetiology of schizophrenia is still unknown but it involves both heritable and non-heritable factors. DNA methylation is an inheritable epigenetic modification that stably alters gene expression. It takes part in the regulation of neurodevelopment and may be a contributing factor to the pathogenesis of brain diseases. It was found that many of the antipsychotic drugs may lead to epigenetic modifications. We have performed 42 high-resolution genome-wide methylation array analyses to determine the methylation status of 27,627 CpG islands. Differentially methylated regions were studied with samples from 20 Bulgarian individuals divided in four groups according to their gender (12 males/8 females) and their treatment response (6 in complete/14 in incomplete remission). They were compared to two age and sex matched control pools (110 females in female pool/110 males in male pool) before and after treatment. We found significant differences in the methylation profiles between male schizophrenia patients with complete remission and control male pool before treatment ( C16orf70 , CST3 , DDRGK1 , FA2H , FLJ30058 , MFSD2B , RFX4 , UBE2J1 , ZNF311 ) and male schizophrenia patients with complete remission and control male pool after treatment ( AP1S3 , C16orf59 , KCNK15 , LOC146336 , MGC16384 , XRN2 ) that potentially could be used as target genes for new therapeutic strategies as well as markers for good treatment response. Our data revealed major differences in methylation profiles between male schizophrenia patients in complete remission before and after treatment and healthy controls which supports the hypothesis that antipsychotic drugs may play a role in epigenetic modifications.